2019•PubMedRequires access

[Baicalein inhibits PI3K/AKT signaling pathway and induces autophagy of MGC-803 cells].

Dan Qiao, Yingshun Li, Jian Xing, Peilin Sun, Ying Wang, Yingying Zhang, Liyan Chen, Xiangshan Ren, Zhenhua Lin, Jingchun Jin, Yingshi Piao

Open publisher page 13 citations

Abstract

Objective To investigate the effect of baicalein (BAI) on autophagy in gastric cancer cell line MGC-803. Methods MGC-803 cells were treated with 0, 5, 15, 25, 50 μmol/L BAI for 24, 48, 72 hours. The proliferation activity of MGC-803 cells was detected by MTT assay. Acridine orange (AO) staining combined with immunofluorescence cytochemical staining was performed to observe the expression of microtubule-associated protein 1 light chain 3 (LC3) and P62 to determine autophagy in MGC-803 cells. The protein levels of LC3, P62, phosphatidylinositol 3-kinase (PI3K), phosphorylated PI3K (p-PI3K), AKT, and p-AKT were detected by Western blot analysis. Results Compared with the control group, BAI significantly inhibited the proliferation of MGC-803 cells in a time- and dose-dependent manner. BAI-treated MGC-803 cells showed a significant increase in acid lysosomes and increased LC3 expression. BAI treatment significantly decreased phosphorylation of PI3K and AKT proteins, increased the ratio of LC3-II/LC3-I and up-regulated the expression of P62 protein. Conclusion Baicalein could inhibit PI3K/AKT signaling pathway and induce autophagy in MGC-803 cells.

About this research paper

What this paper is about

Objective To investigate the effect of baicalein (BAI) on autophagy in gastric cancer cell line MGC-803. Methods MGC-803 cells were treated with 0, 5, 15, 25, 50 μmol/L BAI for 24, 48, 72 hours. The proliferation activity of MGC-803 cells was detected by MTT assay. Acridine orange (AO) staining combined with immunofluorescence cytochemical staining was performed to observe the expression of microtubule-associated protein 1 light chain 3 (LC3) and P62 to determine autophagy in MGC-803 cells. The protein levels of LC3, P62, phosphatidylinositol 3-kinase (PI3K), phosphorylated PI3K (p-PI3K), AKT, and p-AKT were detected by Western blot analysis. Results Compared with the control group, BAI significantly inhibited the proliferation of MGC-803 cells in a time- and dose-dependent manner. BAI-treated MGC-803 cells showed a significant increase in acid lysosomes and increased LC3 expression. BAI treatment significantly decreased phosphorylation of PI3K and AKT proteins, increased the ratio of LC3-II/LC3-I and up-regulated the expression of P62 protein. Conclusion Baicalein could inhibit PI3K/AKT signaling pathway and induce autophagy in MGC-803 cells.

Why it matters

OpenAlex reports 13 citations for this work. Citation counts describe recorded attention and do not establish research quality.

Key contribution

A contribution statement is not available in the OpenAlex record.

Method / approach

Method details are not available in the OpenAlex metadata.

Main findings

Findings are not separately available in the OpenAlex metadata.

Limitations

Limitations are not available in the OpenAlex metadata.

Applications

Application details are not available in the OpenAlex metadata.

Available abstract

Objective To investigate the effect of baicalein (BAI) on autophagy in gastric cancer cell line MGC-803. Methods MGC-803 cells were treated with 0, 5, 15, 25, 50 μmol/L BAI for 24, 48, 72 hours. The proliferation activity of MGC-803 cells was detected by MTT assay. Acridine orange (AO) staining combined with immunofluorescence cytochemical staining was performed to observe the expression of microtubule-associated protein 1 light chain 3 (LC3) and P62 to determine autophagy in MGC-803 cells. The protein levels of LC3, P62, phosphatidylinositol 3-kinase (PI3K), phosphorylated PI3K (p-PI3K), AKT, and p-AKT were detected by Western blot analysis. Results Compared with the control group, BAI significantly inhibited the proliferation of MGC-803 cells in a time- and dose-dependent manner. BAI-treated MGC-803 cells showed a significant increase in acid lysosomes and increased LC3 expression. BAI treatment significantly decreased phosphorylation of PI3K and AKT proteins, increased the ratio of LC3-II/LC3-I and up-regulated the expression of P62 protein. Conclusion Baicalein could inhibit PI3K/AKT signaling pathway and induce autophagy in MGC-803 cells.

Key concepts: Autophagy, PI3K/AKT/mTOR pathway, Protein kinase B, Western blot, Baicalein, Chemistry, Acridine orange, Phosphorylation

Related papers

Back to paper searchBrowse research topicsOriginal source
[Baicalein inhibits PI3K/AKT signaling pathway and induces autophagy of MGC-803 cells]. — Research Paper | ScholarLens